Figure 6.

miR‐145‐5p suppressed AKAP12 to reduce DTX resistance of PCa. A, AKAP12 expression was significantly down‐regulated after miR‐145‐5p was overexpressed in PC3‐DXT cells. B, MTT assay: Increased expression of AKAP12 enforced resistance to DTX and promoted cell proliferation, but increased expression of miR‐145‐5p enforced sensitivity to DTX at the dose of 10 nmol/L DTX. No significant change was observed in miR‐145‐5p and AKAP12 co‐overexpression group. C, TUNEL assay: AKAP12 enhanced the resistance to DTX‐induced apoptosis, but miR‐145‐5p induced the apoptosis of DTX‐resistant cells. No significant change was observed in miR‐145‐5p and AKAP12 co‐overexpression group. Bar: 50 μm. D, Flow cytometry results revealed that AKAP12 impaired the DTX‐induced G2/M arrest of PC3‐DTX cells that was enhanced in miR‐245‐5p group. No significant difference was observed in AKAP12 and miR‐145‐5p simultaneously overexpression group. E, Wound healing assay: AKAP12 induced the migration of chemo‐resistant PCa cells, while miR‐145‐5p inhibited the migration of PC3‐DTX, which was attenuated by AKAP12. Bar: 200 μm. F, Transwell assay: AKAP12 significantly recovered the invasive capacity of PC3‐DTX cells under the treatment of 10 nmol/L DTX, whereas miR‐145‐5p impaired PC3‐DTX invasive capacity. Cotransfected with MALAT1 and miR‐145‐5p mimics, invasive capacity was not significantly changed compared with NC. Bar: 50 μm. NC: negative control. *Compared with control group, P < .05. **Compared with NC group, P < .01